Background

From population-based studies, it is demonstrated that an age-adjusted decrease in manifestations of atherosclerotic cardiovascular diseases such as stroke and coronary heart disease is present over the last decades in high-income countries.[1-5]
The composition of atherosclerotic plaques reflects the local atherosclerotic disease severity. Thin capped atheromatous plaques are associated with rupture resulting in thrombotic occlusion and a subsequent acute cardiovascular event.[6] In addition, a minority of thrombotic events are caused by plaque erosion in the presence of a fibrous lesion.[7]
To investigate time dependent changes in atherosclerotic plaque characteristics, the Athero-Express study was used, and histological features were analyzed of over 1500 plaques removed during carotid endarterectomy from patients with similar symptomatology included from 2002 to 2011.
The analysis included quantification of collagen, calcifications, lipid cores, plaque thrombosis, macrophages, smooth muscle cells, and microvessels.
Athero-Express is an ongoing longitudinal biobank study collecting carotid atherosclerotic plaques from patients that undergo carotid endarterectomy in the University Medical Center Utrecht or the St Antonius Hospital Nieuwegein, the Netherlands.[8]

Main results

The prevalence of plaques with large lipid cores, covering >40% of the plaque surface, were frequently observed in 2002-2003 (33.2%) and less frequently observed in 2010-2011 (14.4%, p<0.001).

The occurrence of plaque thrombosis was more prevalent in the early years (74.4%) as compared to more recent years (37.6%, p=0.001).

Strong fluctuations were observed in macrophage and smooth muscle cell counts between 2002 and 2011. For both cell types the highest values were observed in 2006-2007 and the lowest values were observed in 2010-2011. The median macrophage percentages were 0.41 % in 2002-2003, and 0.09 % in 2011-2012.

Conclusion

Over the past decade, atherosclerotic plaques harvested during carotid endarterectomy show a time dependent change in plaque composition characterized by a decrease in features currently believed to be causal for plaque instability. This seems to go hand in hand with improvements in risk factor management.